BackgroundThe potential application of Ficus deltoidea and vitexin for the management of symptomatologies associated with diabetes mellitus (DM) has gained much attention. However, less firm evidence comes from data to augment our understanding of the role of F. deltoidea and vitexin in protecting pancreatic β-cells. The aim of this study was to assess histological and oxidative stress changes in the pancreas of streptozotocin (STZ)-induced diabetic rats following F. deltoidea extract and vitexin treatment.Methods F. deltoidea and vitexin was administrated orally to six-weeks STZ-induced diabetic rats over 8 weeks period. The glucose and insulin tolerances were assessed by intraperitoneal glucose (2 g/kg) tolerance test (IPGTT) and intraperitoneal insulin (0.65 U/kg) tolerance test (IPITT), respectively. Subsequently, insulin resistance was assessed by homeostasis assessment model of insulin resistance (HOMA-IR), quantitative insulin sensitivity check index (QUICKI) and the insulin/triglyceride-derived McAuley index. The histological changes in the pancreas were then observed by hematoxylin-eosin (H&E) staining. Further, the pattern of fatty acid composition and infrared (IR) spectra of the serum and pancreas were monitored by gas chromatography (GC) method and Fourier Transform Infrared (FT-IR) spectroscopy.Results F. deltoidea and vitexin increased pancreatic antioxidant enzymes and promoted islet regeneration. However, a significant increase in insulin secretion was observed only in rats treated with F. deltoidea. More importantly, reduction of fasting blood glucose is consistent with reduced FT-IR peaks at 1200-1000 cm−1.ConclusionsThese results accentuate that F. deltoidea and vitexin could be a potential agent to attenuate pancreatic oxidative damage and advocate their therapeutic potential for treating DM.

Despite the fact that Ficus deltoidea and vitexin played important roles in controlling hyperglycemia, an effective mitigation strategy dealing with cognitive deficit observed in diabetes, little is known about its neuroprotective effects. The study is aimed to determine changes in behavioral, gyrification patterns and brain oxidative stress markers in streptozotocin (STZ)-induced diabetic rats following F. deltoidea and vitexin treatments. Diabetic rats were treated orally with metformin, methanolic extract of F. deltoidea leaves and vitexin for eight weeks. Morris water maze (MWM) test was performed to evaluate learning and memory functions. The patterns of cortical gyrification were subsequently visualized using micro-computed tomography (micro-CT). Quantification of brain oxidative stress biomarkers, insulin, amylin as well as serum testosterone were measured using a spectrophotometer. The brain fatty acid composition was determined using gas chromatography (GC). Biochemical variation in brain was estimated using Fourier transform infrared (FT-IR) spectroscopy. Results showed that oral administration of F. deltoidea extract and vitexin to diabetic rats attenuated learning and memory impairment, along with several clusters of improved gyrification. Both treatments also caused a significant increase in the superoxide dismutase (SOD) and glutathione peroxidase (GPx) values, as well as a significant reduction of TBARS. Strikingly, improvement of cortical gyrification, spatial learning and memory are supported by serum testosterone levels, fatty acid composition of brain and FT-IR spectra.

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Prenatal hyperparathyroidism (HPT) is one of the true emergency cases and capable of causing serious problems to the mother as well as the unborn baby. This in-vivo study was aimed to investigate the changes in parathyroid hormone (PTH) level of rabbit fetal bodies exposed to diagnostic ultrasound during pregnancy for varying duration of time. As compared to that of control, significantly low PTH levels were observed in the groups exposed for 30 and 60 minutes during pregnancy. This ultrasound heating effect could trigger further studies to look for any adverse effects and/or clinical benefits in human during fetal stage.

Quassinoid-rich EL extract enables to protect against bone loss due to testosterone deficiency. The protective effect on cortical thickness and biomechanical parameters is comparable to testosterone group.